Journal of Infection (1992 ) 25, 67-71
CASE REPORT d u e to Legionella bozemanH a n d C h l a m y d i a psittaci[ TWAR f o l l o w i n g r e n a l t r a n s p l a n t a t i o n
Pneumonia
H. H u m p h r e y s , * ~ R. J. Marshall,* I. M a c k a y t a n d E. O. Caul~
Departments of * Microbiology and ~fRenal Medicine, Southmead Hospital, Westbury-on-Trym, Bristol BSIo 5NB and ~ Public Health Laboratory, Myrtle Road, Kingsdown, Bristol BS2 8EL, U.K. Accepted for publication I I November 1991 Summary
Chlamydia and Legionella are recognised causes of atypical pneumonia. A case of pneumonia due to Chlamydia psittaci/TWAR and Legionella bozemanii following renal transplantation is described. Legionella bozemanii infection was diagnosed by a rise in antibodies and by isolation of the organism from bronchoscopy specimens. It is unusual to find pneumonia caused concomitantly by two such agents. This case, despite the fatal outcome, emphasises the necessity for a comprehensive approach to the diagnosis of atypical pneumonia, including culture for Legionella, especially in immunocompromised patients. Introduction Infection is an important complication of renal transplantation and respiratory tract infection due to legionella must be considered in such p a t i e n t s ) Legionella bozemanii was first described in I968 and was initially regarded as a rickettsia-like agent. 2 It is environmental in origin but has been implicated as a cause of p n e u m o n i a in the i m m u n o s u p p r e s s e d p a t i e n t ) Most routine serological investigations u n d e r t a k e n to diagnose atypical p n e u m o n i a will not detect it as a cause of respiratory tract infection. It can, however, be isolated from the respiratory tract if optimal specimens are taken and cultured appropriately. We report a case of p n e u m o n i a due to chlamydia in a patient following renal transplantation f r o m w h o m we also isolated L. bozemanii.
Case report A 5o-year-old w o m a n was admitted to hospital with increasing breathlessness and fever for 48 h. One m o n t h previously she had u n d e r g o n e renal transplantation for end-stage renal failure considered to be due to analgesic nephropathy. Renal biopsy on day 6 after transplantation showed tubular necrosis and on day 14, moderately severe cellular rejection. This was treated with azathioprine, high dose steroids and cyclosporin A and the patient was eventually discharged f r o m hospital. O n admission 2 days later she had a Address correspondence to: Dr H. Humphreys, Department of Microbiology, University Hospital, Queen's Medical Centres, Nottingham NG7 2Ut-I, U.K. o163-4453/92/o4oo67+o5 $03.00/o
© 1992 The British Society for the Study of Infection 3-2
68
H. H U M P H R E Y S
ET AL.
temperature of 40 °C, a tachycardia of i2o min and was tachypnoeic at rest. Clinical and radiological evidence suggested a right upper lobe p n e u m o n i a and she was c o m m e n c e d on ampicillin, 5o0 m g Iv 6 hourly. Initial investigations included a haemoglobin of 7"5 (Io'5-I5"o) g/dl, and Vc'BC count of 3"2 x io9/1 (4"o-I i) with 55 % neutrophils. Her urea was I4"8 (2"I-7"o) mmol/1, potassium 4"I (3"3-4"8)mmol/1, creatinine I96 (5o--I2O)#mol/1 and creatinine clearance I9 m l / m i n . Blood cultures taken on admission were sterile and s p u t u m processed for conventional bacterial pathogens grew upper respiratory tract flora only. T w o days later she was transferred to the intensive therapy unit for mechanical ventilation. She remained pyrexial and chest X-ray showed shadowing of the upper, middle and lower lobes of the right lung. Her antibiotic therapy was changed to cefuroxime 750 mg iv 8 hourly and erythromycin 500 m g IV 6 hourly to treat a possible atypical p n e u m o n i a and this was continued for 3 weeks. T w o weeks after the change in therapy she still required mechanical ventilation, haemodialysis and total parenteral nutrition. She eventually recovered sufficiently to be transferred off the intensive care unit. However an abscess cavity remained in her right middle lobe and continued to act as a septic focus. She then developed an Enterobacter cloacae septicaemia, deteriorating respiratory function and renal transplant rejection. As the patient had previously been suicidal while on dialysis, it was decided to maintain her immunosuppressive therapy, albeit in reduced dosage, to avoid having to resort once again to dialysis to manage her renal failure. Forty-eight days after admission to hospital she died of unresolving sepsis, partly contributed to by immunosuppressive therapy necessary to control kidney rejection. P o s t - m o r t e m examination revealed a necrotic right middle lobe with fibrinous pleurisy. She had cystic changes in her own host kidneys and swelling, with cellular rejection and autolysis of tubular cells, in the transplanted kidney. Respiratory specimens taken at bronchoscopy and placed in sterile normal saline 2 days after admission were negative by immunofluorescence and culture for a variety of viral respiratory pathogens. Legionella pneurnophila antigen was not detected by direct immunofluorescence but 3 days after incubation in 5 % carbon dioxide, Gram-negative rods were isolated on Legionella CYE agar base (Oxoid, U.K.) containing Growth and Selective Supplements (Oxoid, U.K.). Immunofluorescent serology examination indicated that this bacterium was either L. bozernanii serogroup I or Legionella parisiensis. Restriction fragment length polymorphism (RFLP) confirmed the isolate as L. bozemanii. Serum samples were tested for antibodies to organisms causing atypical p n e u m o n i a including indirect immunofluorescent antibody to legionella and the results are outlined in Table I according to the date of onset of symptoms. Absorption was performed by the m e t h o d previously described 4 using Escherichia coli N C T C IO418. Antibodies to L. bozemanii were detected in serum taken 4 days after the initial onset of symptoms (titre, 512) compared with none in serum taken 7 days before and retrospectively tested. Although there was a rise in complement fixing antibodies to Mycoplasrna pneumoniae there was no specific I g M response. T h e r e was serological evidence of
L e g i o n e l l a and C h l a m y d i a pneumonia
69
T a b l e I Serological investigations to diagnose atypical pneumonia Titres 3 days before onset
Titres 4 days after onset
Titres 13 days after onset
Titres 36 days after onset
< i6 < 8
< I6 < 8
< 16 < 8
< I6 < 8
< 16 < 16
512 512
lO24 1024
256 256
Complement fixation CF after absorption IgM
< 16 < I6
CASE REPORT d u e to Legionella bozemanH a n d C h l a m y d i a psittaci[ TWAR f o l l o w i n g r e n a l t r a n s p l a n t a t i o n
Pneumonia
H. H u m p h r e y s , * ~ R. J. Marshall,* I. M a c k a y t a n d E. O. Caul~
Departments of * Microbiology and ~fRenal Medicine, Southmead Hospital, Westbury-on-Trym, Bristol BSIo 5NB and ~ Public Health Laboratory, Myrtle Road, Kingsdown, Bristol BS2 8EL, U.K. Accepted for publication I I November 1991 Summary
Chlamydia and Legionella are recognised causes of atypical pneumonia. A case of pneumonia due to Chlamydia psittaci/TWAR and Legionella bozemanii following renal transplantation is described. Legionella bozemanii infection was diagnosed by a rise in antibodies and by isolation of the organism from bronchoscopy specimens. It is unusual to find pneumonia caused concomitantly by two such agents. This case, despite the fatal outcome, emphasises the necessity for a comprehensive approach to the diagnosis of atypical pneumonia, including culture for Legionella, especially in immunocompromised patients. Introduction Infection is an important complication of renal transplantation and respiratory tract infection due to legionella must be considered in such p a t i e n t s ) Legionella bozemanii was first described in I968 and was initially regarded as a rickettsia-like agent. 2 It is environmental in origin but has been implicated as a cause of p n e u m o n i a in the i m m u n o s u p p r e s s e d p a t i e n t ) Most routine serological investigations u n d e r t a k e n to diagnose atypical p n e u m o n i a will not detect it as a cause of respiratory tract infection. It can, however, be isolated from the respiratory tract if optimal specimens are taken and cultured appropriately. We report a case of p n e u m o n i a due to chlamydia in a patient following renal transplantation f r o m w h o m we also isolated L. bozemanii.
Case report A 5o-year-old w o m a n was admitted to hospital with increasing breathlessness and fever for 48 h. One m o n t h previously she had u n d e r g o n e renal transplantation for end-stage renal failure considered to be due to analgesic nephropathy. Renal biopsy on day 6 after transplantation showed tubular necrosis and on day 14, moderately severe cellular rejection. This was treated with azathioprine, high dose steroids and cyclosporin A and the patient was eventually discharged f r o m hospital. O n admission 2 days later she had a Address correspondence to: Dr H. Humphreys, Department of Microbiology, University Hospital, Queen's Medical Centres, Nottingham NG7 2Ut-I, U.K. o163-4453/92/o4oo67+o5 $03.00/o
© 1992 The British Society for the Study of Infection 3-2
68
H. H U M P H R E Y S
ET AL.
temperature of 40 °C, a tachycardia of i2o min and was tachypnoeic at rest. Clinical and radiological evidence suggested a right upper lobe p n e u m o n i a and she was c o m m e n c e d on ampicillin, 5o0 m g Iv 6 hourly. Initial investigations included a haemoglobin of 7"5 (Io'5-I5"o) g/dl, and Vc'BC count of 3"2 x io9/1 (4"o-I i) with 55 % neutrophils. Her urea was I4"8 (2"I-7"o) mmol/1, potassium 4"I (3"3-4"8)mmol/1, creatinine I96 (5o--I2O)#mol/1 and creatinine clearance I9 m l / m i n . Blood cultures taken on admission were sterile and s p u t u m processed for conventional bacterial pathogens grew upper respiratory tract flora only. T w o days later she was transferred to the intensive therapy unit for mechanical ventilation. She remained pyrexial and chest X-ray showed shadowing of the upper, middle and lower lobes of the right lung. Her antibiotic therapy was changed to cefuroxime 750 mg iv 8 hourly and erythromycin 500 m g IV 6 hourly to treat a possible atypical p n e u m o n i a and this was continued for 3 weeks. T w o weeks after the change in therapy she still required mechanical ventilation, haemodialysis and total parenteral nutrition. She eventually recovered sufficiently to be transferred off the intensive care unit. However an abscess cavity remained in her right middle lobe and continued to act as a septic focus. She then developed an Enterobacter cloacae septicaemia, deteriorating respiratory function and renal transplant rejection. As the patient had previously been suicidal while on dialysis, it was decided to maintain her immunosuppressive therapy, albeit in reduced dosage, to avoid having to resort once again to dialysis to manage her renal failure. Forty-eight days after admission to hospital she died of unresolving sepsis, partly contributed to by immunosuppressive therapy necessary to control kidney rejection. P o s t - m o r t e m examination revealed a necrotic right middle lobe with fibrinous pleurisy. She had cystic changes in her own host kidneys and swelling, with cellular rejection and autolysis of tubular cells, in the transplanted kidney. Respiratory specimens taken at bronchoscopy and placed in sterile normal saline 2 days after admission were negative by immunofluorescence and culture for a variety of viral respiratory pathogens. Legionella pneurnophila antigen was not detected by direct immunofluorescence but 3 days after incubation in 5 % carbon dioxide, Gram-negative rods were isolated on Legionella CYE agar base (Oxoid, U.K.) containing Growth and Selective Supplements (Oxoid, U.K.). Immunofluorescent serology examination indicated that this bacterium was either L. bozernanii serogroup I or Legionella parisiensis. Restriction fragment length polymorphism (RFLP) confirmed the isolate as L. bozemanii. Serum samples were tested for antibodies to organisms causing atypical p n e u m o n i a including indirect immunofluorescent antibody to legionella and the results are outlined in Table I according to the date of onset of symptoms. Absorption was performed by the m e t h o d previously described 4 using Escherichia coli N C T C IO418. Antibodies to L. bozemanii were detected in serum taken 4 days after the initial onset of symptoms (titre, 512) compared with none in serum taken 7 days before and retrospectively tested. Although there was a rise in complement fixing antibodies to Mycoplasrna pneumoniae there was no specific I g M response. T h e r e was serological evidence of
L e g i o n e l l a and C h l a m y d i a pneumonia
69
T a b l e I Serological investigations to diagnose atypical pneumonia Titres 3 days before onset
Titres 4 days after onset
Titres 13 days after onset
Titres 36 days after onset
< i6 < 8
< I6 < 8
< 16 < 8
< I6 < 8
< 16 < 16
512 512
lO24 1024
256 256
Complement fixation CF after absorption IgM
< 16 < I6
